Why does lower blood calcium levels (or lower calcium levels in ECF) cause nervous hyperexcitaton? Why does it cause over stimulation of nerves and muscles and spasmic contractions of muscles?
This is why undersecretion of parathormone causes parathyroid tetany.
I am aware of the role of calcium in opening the synaptic vesicles for transmission of impulses and the role of calcium in muscle contraction but fail to understand how that might hep me understand the overexcitation of nerves and spasmic contraction of muscles. It actually seems that higher calcium in ECF might cause over stimulation and spasms of muscles due to sustained contraction.

2 Answers
2

It is a question of transmembrane potential. Ca++ being a cation, means that if you decrease the amount of ionized calcium in the extra cellular fluid, it conceptually is nearly equivalent to having a more positively charged intracellular fluid. This in turn means that the cell will be closer to its threshold potential for depolarization, therefore accounting for its hyper excitability.

What you should keep in mind, is that when we say something as: "this cell has a transmembrane potential of -70 mV", we always define it relatively to the extra cellular fluid.

Acute hypocalcemia directly increases peripheral neuromuscular irritability [ 1 ]. As measured electromyographically, tetany consists of repetitive high-frequency discharges after a single stimulus. Hyperexcitability of peripheral neurons is probably the most important pathophysiologic effect of hypocalcemia, but hyperexcitability occurs at all levels of the nervous system, including motor end-plates, the spinal reflexes, and the central nervous system.

Guyton and Hall Textbook of Physiology:

The concentration of
calcium ions in the extracellular fluid also has a profound
effect on the voltage level at which the sodium
channels become activated. When there is a deficit of
calcium ions, the sodium channels become activated
(opened) by very little increase of the membrane potential
from its normal, very negative level. Therefore, the
nerve fiber becomes highly excitable, sometimes discharging
repetitively without provocation rather than
remaining in the resting state. In fact, the calcium ion
concentration needs to fall only 50 per cent below
normal before spontaneous discharge occurs in some
peripheral nerves, often causing muscle “tetany.”This is
sometimes lethal because of tetanic contraction of the
respiratory muscles.

The probable way in which calcium ions affect the
sodium channels is as follows:These ions appear to bind
to the exterior surfaces of the sodium channel protein
molecule. The positive charges of these calcium ions
in turn alter the electrical state of the channel protein
itself, in this way altering the voltage level required to
open the sodium gate.